Wonhee Cho, Jeongjin Park, Minhee Lee, Seong-Hoo Park, Jaeeun Jung, Jinhak Kim, Sangwon Eun, and Jinkyung Kim. Prev Nutr Food Sci 2023;28:50-60. https://doi.org/10.3746/pnf.2023.28.1.50

Minhee Lee, Dakyung Kim, Seong-Hoo Park, Jaeeun Jung, Wonhee Cho, A Ram Yu, and Jeongmin Lee. Prev Nutr Food Sci 2022;27:423-35. https://doi.org/10.3746/pnf.2022.27.4.423

Jaeeun Jung, Minhee Lee, Seong-Hoo Park, Wonhee Cho, Jinhak Kim, Sangwon Eun, and Jeongmin Lee. Prev Nutr Food Sci 2024;29:125-34. https://doi.org/10.3746/pnf.2024.29.2.125

The excessive storage of triglycerides in adipose tissue is a characteristic feature of obesity, which arises from an imbalance between energy intake and expenditure. In this study, we aimed to explore the potential anti-obesity effects of Salacia reticulata extracts (SC) in a high-fat diet (HFD)-induced in obese mice and 3T3-L1 adipocytes, with a specific focus on understanding the underlying lipid mechanisms. Mice were fed with a normal diet (NC; normal control), HFD (60% high-fat diet), Met (HFD containing metformin 250 mg/kg b.w.), SC25 (HFD containing SC 25 mg/kg b.w.), SC50 (HFD containing SC 50 mg/kg b.w.), or SC 100 (HFD containing SC 100 mg/kg b.w.) for 12 weeks. Notably, SC supplementation led to significant reductions in body weight gain, adipose tissue weight, adipose tissue mass, and adipocyte size in HFD-fed mice. Furthermore, SC supplementation exerted inhibitory effects on the adipogenesis and lipogenesis pathways while promoting lipolysis and thermogenesis pathways in the adipose tissues of HFD-fed mice. In vitro experiments using 3T3-L1 cells demonstrated that SC treatment during the differentiation phase suppressed adipogenesis and lipogenesis, whereas SC treatment after differentiation, activated lipolysis and thermogenesis. Collectively, these findings indicate that SC exhibits a direct influence on the lipid metabolism of adipocytes, making it an effective candidate for weight loss interventions.

In this study, we investigated the binding of 10 strains of lactic acid bacteria (LAB) to HT29 cells (a human colorectal adenocarcinoma cell line) and aflatoxin B 1 (AFB 1) and the possibility that HT29 cells and AFB 1 compete for the binding site of LAB. All the 10 strains examined showed binding to HT29 cells and AFB 1 , among which Lactobacillus plantarum KCTC 3099 showed the highest binding to both HT29 cells and AFB1. When the binding between L. plantarum KCTC 3099 and HT29 cells was observed in the presence of various concentrations of AFB 1 , the binding was reduced in a concentration-dependent manner, indicating that HT29 cells and AFB 1 compete for the same binding sites in L. plantarum KCTC 3099. The protoplast of L. plantarum KCTC 3099 or HCL-treated L. plantarum KCTC 3099 whose cell wall structure was changed by acid treatment did not show binding to them, suggesting that the cell wall was involved in the binding. In addition, of plantarum KCTC 3099 treated with lipase, pronase E, sodium, m-periodate or urea, m-periodate-treated L. plantarum KCTC 3099 showed the lowest biding to both HT cells and AFB 1. m-Periodate is known to change the OH groups of carbohydrates. These results suggest that 1) HT29 cells and AFB 1 bind to the same site in the cell wall of L. plantarum KCTC, 2) the binding site contains mainly polysaccharide components and importantly 3) biding of L. plantarum KCTC to AFB 1 could reduce the amount of free AFB 1 and thus, the opportunity for AFB 1 to interact with the enterocytes. The binding of LAB to AFB 1 is thought to be the mechanism of anti-toxic or anti-carcinogenic action of LAB probiotics against AFB 1 .

This study aims to evaluate the anti-obesity effects of Ashwagandha (Withania somnifera, AS), Chrysanthemum zawadskii Herbich var. latilobum (Maxim.) Kitamura (C), and their combination (AS:C = 3:1, ASC) in high-fat-diet (HFD)-induced obese animal models. Key metabolic parameters, including body weight, lipid metabolism, adipogenesis, energy expenditure, and glucose homeostasis, were assessed. HFD-fed mice were supplemented with AS25, C25, or ASC at different concentrations (ASC25, ASC50, and ASC100). Body weight, food efficiency ratio (FER), organ and adipose tissue weights were measured. Serum biochemical markers, including lipid profiles, glucose, insulin, and liver enzymes, were analyzed. Western blot analysis was conducted to assess the expression of key proteins involved in adipogenesis, lipogenesis, lipolysis, and energy metabolism. ASC complex supplementation, particularly at higher doses (ASC100), significantly reduced body weight gain, liver weight, and total white adipose tissue (WAT) accumulation. ASC complex groups exhibited improved lipid profiles, with reductions in triglycerides, total cholesterol, and low-density lipoprotein (LDL). Serum glucose, insulin, and HbA1c levels were significantly reduced, suggesting improved insulin sensitivity. Western blot analysis revealed that ASC complex supplementation downregulated key adipogenic markers, including PPARγ, C/EBPα, and SREBP1c, while enhancing adiponectin levels. ASC complex also promoted energy metabolism by increasing the phosphorylation of AMPK and UCP1 expression, indicative of enhanced thermogenesis and lipid oxidation. ASC complex supplementation demonstrates a potent anti-obesity effect by modulating adipogenesis, lipid metabolism, and energy expenditure. The findings suggest that ASC complex could serve as a promising natural therapeutic strategy for obesity and metabolic disorders. Further research, including clinical trials, is warranted to validate its efficacy and safety in human populations.